The effect of eight weeks resistance and aerobic training on myostatin and follistatin expression in cardiac muscle of rats

Abstract

Introduction: The clinical studies have shown that the myostatin gene expression and its serum density occur more frequently in heart patients than in healthy individuals. The purpose of this study is to investigate the influence of 8-week resistance and aerobic exercise on the myostatin and follistatin gene expression of myocardium muscle of healthy male Wistar rats. Methods: In this experimental study, 20 five-week-old adult Wistar rats (250 ± 26.5 g) were divided into three groups: healthy control group (n = 6), resistance exercise group (n = 7), and aerobic exercise group (n = 7). The resistance and aerobic exercise plan consisted of 8 weeks and 3 sessions per week. The resistance exercise group performed climbing a one-meter 26-stair ladder with a slope of 85 degrees for 3 sets of 5 repetitions per session. The aerobic exercise group performed running at a speed of 12 meters per minute for 30 minutes during the first sessions gradually increasing up to a speed of 30 meters per minute for 60 minutes during the final sessions (equivalent to 70% to 80% of maximum oxygen consumption). The differences between the groups were evaluated using a one-way analysis of variance (ANOVA) test. When appropriate, LSD post-hoc test was used. The significance level for the study was less than 0.05. Results: The results of this study shows that after 8 weeks of exercise, there is no significant difference between myostatin mRNA gene expression levels of the heart muscle among the three groups of control, resistance exercise, and aerobic exercise (P = 0.172, F = 1.953). However, the mean differences between follistatin mRNA levels of the heart muscle among the three groups of control, resistance exercise, and aerobic exercise are statistically significant (F = 38.022, P = 0.001). Furthermore, the ratio of follistatin to myostatin mRNA gene expression of the heart muscle (P = 0.001, F = 10.288) shows significant difference among the three groups. Conclusion: Our results indicate that the resistance and aerobic exercise could cause a decrease in myostatin and an increase in follistatin levels, thus preventing many muscular physiological disorders such as arthritis and muscle weakness.

Effects of 8 Weeks of Resistance Training and IGF-1 Injection on Biochemical Markers of Cancer and Colorectal Structures in Rats

“…Subjects in the C and II groups did not perform any exercise. Subjects in the II and RI groups received intramuscular IGF-I injection in the left calf and tibialis anterior muscles before and after the exercise sessions (1.5 µg/Kg per day) (23). Rats in the RS and C groups received intramuscular saline injection at comparable times and doses.…”

Myostatin and the Heart

“…However, it markedly elevated heart mRNA follistatin expression. As a result, the ratio of follistatin mRNA/myostatin mRNA increased considerably [59]. Because follistatin is an inhibitor of myostatin, such a shift in follistatin/myostatin balance would facilitate the heart hypertrophy in the course of training.…”

Modern conception of myostatin biological role and clinical significance as the main regulator of muscle growth and differentiation

“…Достаточно большое количество исследований посвящено изучению активности миостатина у больных с хронической сердечной недостаточностью (ХСН), так как кардиальная кахексия является независимым фактором риска смертности [25]. Имеются противоречивые данные о связи уровня миостатина в плазме с развитием ХСН: в некоторых работах показано повышение уровня миостатина у таких больных [26], в других, наоборот, наблюдалось снижение концентрации данного белка у пациентов с сердечной недостаточностью [27] возможно, не противоречат друг другу: эти различия могут быть связаны с разными стадиями заболевания или же с генетическими различиями популяций пациентов, изучаемых в разных работах. Как было отмечено, миостатин стимулирует деление фибробластов.…”

“…Есть исследования, в которых показано, что курение нарушает процесс синтеза мышечного белка и, вероятно, повышает риск развития саркопении [47]. Физические упражнения, самостоятельно или в составе комплексной терапии, приводят к снижению плазменной концентрации миостатина и повышению мышечной массы [48,49]. Постоянная гипоксия и окислительный стресс, сопровождающиеся накоплением активных форм кислорода [50], способствуют индукции синтеза миостатина.…”